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THE ROLE OF ACQUIRED IMMUNITY AND PERIODONTAL DISEASE PROGRESSION

^* Division of Periodontics, School of Dentistry, and Department of Microbiology & Immunology, Faculty of Medicine & Dentistry, the University of Western Ontario, London, Ontario N6A 5C1, Canada; Lawson Health Research Institute, London Health Sciences Centre, London, Ontario N6A 4G5; and Division of Periodontics, Eastman Dental Clinic, Center for Oral Biology, and Dept. of Microbiology and Immunology, School of Medicine & Dentistry, University of Rochester, NY, USA 14620-2989;

View larger version (36K): [in a new window]   Figure 1. Expression of RANK-L on A. actinomycetemcomitans-reactive periodontal CD4+ T-cells detected by flow cytometry and PCR analyses. The left panel (FACS analysis of RANK-L expression on cell surface by immunostaining to OPG-FITC conjugates): (a) un-stimulated HuPBL-derived CD4+ T-cells as background control; (b) isotypic Ig control for background staining; (c) HuPBL-derived CD4+ T-cells activated by anti-h-ßTCR plus anti-CD28 Mabs as positive control for RANK-L expression; and (d) periodontal CD4+ T-cells stained with OPG-FITC for cell-surface expression of RANK-L. The right panel (RT-PCR by the use of specific primers for RANK-L): (1) A. actinomycetemcomitans (Aa)-reactive periodontal CD4+ T-cells from HuPBL-NOD/SCID mice which received HuPBL samples from one LJP subject (called LJP 2); (2) Aa-reactive periodontal CD4+ T-cells from HuPBL-NOD/SCID mice which received HuPBL samples from another LJP subject (called LJP 1); (3) naïve unstimulated HuPBL-derived CD4+ T-cells; and (4) HuPBL-derived CD4+ T-cells activated by anti-h-ßTCR plus anti-CD28 mAbs as positive control for RANK-L expression. The experimental procedures have been described previously (Teng et al., 2000; Teng, 2002).

View larger version (36K): [in a new window]   Figure 2. Interaction of CD4+ T-cells and alveolar bone remodeling in the periodontium. After being challenged by periodontal pathogens through antigen processing and presentation (via APC-dendritic cells, macrophages, activated B-cells, etc.), these micro-organisms-specific periodontal CD4+ T-cells become activated and produce RANK-L molecules. RANK-L can activate osteoclasts (OC) directly to induce bone resorption and also induce the differentiation, survival, and activation of OC precursors. OPG, the natural decoy receptor of RANK-L produced by the stromal cells (i.e., osteoblasts, chondrocytes), can compete for the binding to RANK-L molecules, thereby counteracting the effects of RANK-L/RANK signaling on OC and OC precursors.